Effect of prolonged gastric distension on motor  function of LES and of proximal stomach

Gastric distension is a potent stimulus of transient lower esophageal sphincter (LES) relaxation. To investigate the time effect of prolonged gastric distension on the rate of transient LES relaxations, LES pressure, and the motor and sensory functions of the proximal stomach, we performed a continuous isobaric distension of the proximal stomach at the 75% threshold pressure for discomfort for 2 h in seven healthy subjects. A multilumen assembly incorporating a sleeve and an electronic barostat was used. The rate of transient LES relaxations ( n/30 min) was constant during the first hour [4.1 ± 1.2 (0–30 min) and 5.4 ± 1.1 (30–60 min)] but markedly decreased ( P < 0.05) in the second hour [2.1 ± 0.5 (60–90 min) and 2.3 ± 0.9 (90–120 min)], whereas LES pressure, baseline volume and volume waves within the gastric bag, hunger, and fullness did not change throughout the experiment. It is concluded that the rate of transient LES relaxations decreases with time during prolonged gastric distension, thus suggesting that this type of stimulus should not be used in sequential experimental conditions.

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H. pylori and transient lower esophageal sphincter relaxations induced by gastric distension in healthy humans

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.281.2.g350 ◽

2001 ◽

Vol 281 (2) ◽

pp. G350-G356 ◽

Cited By ~ 17

Author(s):

Frank Zerbib ◽

Valérie Bicheler ◽

Véronique Leray ◽

Madeleine Joubert ◽

Stanislas Bruley des Varannes ◽

...

Keyword(s):

Helicobacter Pylori ◽

Lower Esophageal Sphincter ◽

Proinflammatory Cytokine ◽

Healthy Subjects ◽

Gastric Distension ◽

Healthy Humans ◽

Biopsy Specimens ◽

Esophageal Sphincter ◽

H Pylori

The role of Helicobacter pylori infection in the control of lower esophageal sphincter (LES) motility, especially the occurrence of transient LES relaxations (TLESRs), was studied in eight H. pylori-positive and eight H. pylori-negative healthy subjects. During endoscopy, biopsy specimens were taken from the cardia, fundus, and antrum for determinations of H. pyloristatus, gastritis, and proinflammatory cytokine mucosal concentrations. LES motility was monitored during three different 30-min periods: baseline, gastric distension (barostat), and gastric distension with CCK infusion. Gastric distension significantly increased the TLESR rate, whereas CCK increased the rate of distension-induced TLESRs further and reduced resting LES pressure without significant differences between infected and noninfected subjects. H. pylori status did not influence resting LES pressure or gastric compliance. Cytokine mucosal concentrations were increased in infected patients, but no correlation was found with the TLESR rate, which was also independent of inflammation at the cardia, fundus, and antrum. These results suggest that H. pylori-associated inflammation does not affect the motor events involved in the pathogenesis of gastroesophageal reflux.

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Response of canine lower esophageal sphincter to gastric distension

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1990.259.3.g380 ◽

1990 ◽

Vol 259 (3) ◽

pp. G380-G385 ◽

Cited By ~ 11

Author(s):

S. J. Franzi ◽

C. J. Martin ◽

M. R. Cox ◽

J. Dent

Keyword(s):

Lower Esophageal Sphincter ◽

Gastric Wall ◽

Progressive Increase ◽

Truncal Vagotomy ◽

Gastric Distension ◽

Wall Tension ◽

Proximal Stomach ◽

Lower Esophageal Sphincter Relaxation ◽

Esophageal Sphincter ◽

Antral Distension

The aim of this study was to localize the region of the stomach responsible for triggering distension-induced transient lower esophageal sphincter relaxation (TLESR). The canine stomach was partitioned into subsegments by a row of buttressed sutures. This separated either the fundus from the lesser curve or the proximal stomach from the antrum. After 1 mo each region was progressively distended while gastroesophageal pressures were monitored. At the time of the first TLESR, gastric wall tension was estimated from the bag pressure and volume. Distension of the intact stomach, lesser curve, or proximal stomach in 12 dogs produced a progressive increase in lower esophageal sphincter (LES) pressure, which was interrupted at low gastric wall tension (29, 35, and 40 mmHg.cm, respectively) by a superimposed TLESR. Background LES pressure fell progressively with distension of the antrum but was unchanged by distension of the fundus alone. Both the fundus and antrum had significantly higher thresholds for triggering TLESR (96 and 105 mmHg.cm). In another two dogs truncal vagotomy performed at the time of gastric partitioning prevented both the change in background LES pressure, and the triggering of TLESR, associated with proximal gastric and antral distension. We conclude that the subcardiac region of the stomach is primarily responsible for triggering TLESR induced by distension and that the effect on background LES pressure depends on the region distended.

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Distension of the esophagogastric junction augments triggering of transient lower esophageal sphincter relaxation

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00523.2010 ◽

2011 ◽

Vol 301 (4) ◽

pp. G713-G718 ◽

Cited By ~ 8

Author(s):

Michiel P. van Wijk ◽

L. Ashley Blackshaw ◽

John Dent ◽

Marc A. Benninga ◽

Geoffrey P. Davidson ◽

...

Keyword(s):

Healthy Volunteers ◽

Lower Esophageal Sphincter ◽

Healthy Subjects ◽

Esophagogastric Junction ◽

Vagal Afferents ◽

Gastric Distension ◽

Adaptation Period ◽

Baseline Recording ◽

Exact Position ◽

Esophageal Sphincter

Patients with gastroesophageal reflux disease show an increase in esophagogastric junction (EGJ) distensibility and in frequency of transient lower esophageal sphincter relaxations (TLESR) induced by gastric distension. The objective was to study the effect of localized EGJ distension on triggering of TLESR in healthy volunteers. An esophageal manometric catheter incorporating an 8-cm internal balloon adjacent to a sleeve sensor was developed to enable continuous recording of EGJ pressure during distension of the EGJ. Inflation of the balloon doubled the cross-section of the trans-sphincteric portion of the catheter from 5 mm OD (round) to 5 × 11 mm (oval). Ten healthy subjects were included. After catheter placement and a 30-min adaptation period, the EGJ was randomly distended or not, followed by a 45-min baseline recording. Subjects consumed a refluxogenic meal, and recordings were made for 3 h postprandially. A repeat study was performed on another day with EGJ distension status reversed. Additionally, in one subject MRI was performed to establish the exact position of the balloon in the inflated state. The number of TLESR increased during periods of EGJ distension with the effect being greater after a meal [baseline: 2.0(0.0–4.0) vs. 4.0(1.0–11.0), P=0.04; postprandial: 15.5(10.0–33.0) vs. 22.0(17.0–58.0), P=0.007 for undistended and distended, respectively]. EGJ distension augments meal-induced triggering of TLESR in healthy volunteers. Our data suggest the existence of a population of vagal afferents located at sites in/around the EGJ that may influence triggering of TLESR.

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Tension receptors in the proximal stomach: Are they relevant to triggering of transient lower esophageal sphincter relaxations (TLESRs)?

Gastroenterology ◽

10.1016/s0016-5085(01)82154-5 ◽

2001 ◽

Vol 120 (5) ◽

pp. A434-A434

Author(s):

S CAMAGNOLA ◽

P CANTU ◽

M ALLOCCA ◽

P BIANCHI ◽

R PENAGINI

Keyword(s):

Lower Esophageal Sphincter ◽

Proximal Stomach ◽

Esophageal Sphincter

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Effect of hyperglycemia on triggering of transient lower esophageal sphincter relaxations

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00383.2003 ◽

2004 ◽

Vol 286 (5) ◽

pp. G797-G803 ◽

Cited By ~ 19

Author(s):

Qing Zhang ◽

Michael Horowitz ◽

Rachael Rigda ◽

Christopher Rayner ◽

Andrew Worynski ◽

...

Keyword(s):

Diabetes Mellitus ◽

Lower Esophageal Sphincter ◽

Blood Glucose Concentration ◽

Gastric Wall ◽

Gastric Distension ◽

Healthy Human ◽

Patients With Diabetes ◽

Esophageal Sphincter ◽

Volume Controlled ◽

Pressure Controlled

Acute changes in blood glucose concentration have major effects on gastrointestinal motor function. Patients with diabetes mellitus have an increased prevalence of gastroesophageal reflux. Transient lower esophageal sphincter (LES) relaxation (TLESR) is the most common sphincter mechanism underlying reflux. The aim of this study was to investigate the effect of acute hyperglycemia on triggering TLESRs evoked by gastric distension in healthy volunteers. TLESRs were stimulated by pressure-controlled and volume-controlled (500 ml) gastric distension using an electronic barostat and performed on separate days. On each day, esophageal manometry was performed in the sitting position during gastric distension for 1 h under euglycemia (5 mM), and either marked hyperglycemia (15 mM) or physiological hyperglycemia (8 mM) in randomized order was maintained by a glucose clamp. Marked hyperglycemia doubled the rate of TLESRs in response to both pressure-controlled [5 (3–10.5, median or interquartile range) to 10 (9.5–14.5) per hour, P < 0.02] and volume-controlled [4 (2.5–7.5) to 10.5 (7–12.5) per hour, P < 0.02] gastric distension but had no effect on basal LES pressure. Physiological hyperglycemia had no effect on the triggering of TLESRs or basal LES pressure. In healthy human subjects, marked hyperglycemia increases the rate of TLESRs. Increase in the rate of TLESRs is independent of proximal gastric wall tension. Mechanisms underlying the effect remain to be determined. Hyperglycemia may be an important factor contributing to the increased esophageal acid exposure in patients with diabetes mellitus.

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Relation between proximal stomach pressure and transient lower esophageal sphincter relaxations

European Journal of Gastroenterology & Hepatology ◽

10.1097/00042737-199812000-00260 ◽

1998 ◽

Vol 10 (12) ◽

pp. A82

Author(s):

R. C.H. Scheffer ◽

J. E. Bais ◽

L. M.A. Akkermans ◽

H. G. Gooszen

Keyword(s):

Lower Esophageal Sphincter ◽

Proximal Stomach ◽

Esophageal Sphincter

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Diaphragmatic contribution to gastroesophageal competence and reflux in dogs

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1992.263.4.g551 ◽

1992 ◽

Vol 263 (4) ◽

pp. G551-G557 ◽

Cited By ~ 9

Author(s):

C. J. Martin ◽

W. J. Dodds ◽

H. H. Liem ◽

R. O. Dantas ◽

R. D. layman ◽

...

Keyword(s):

Gastroesophageal Reflux ◽

Lower Esophageal Sphincter ◽

Short Duration ◽

Gastroesophageal Junction ◽

Selective Inhibition ◽

High Amplitude ◽

Gastric Distension ◽

Esophageal Body ◽

Esophageal Sphincter ◽

Crural Diaphragm

Events associated with gastroesophageal reflux have been determined by concurrent diaphragmatic and esophageal body electromyography, video radiography, and manometry in four conscious dogs. Three characteristic phenomena occurred in parallel immediately before and during gastroesophageal reflux: 1) transient lower esophageal sphincter relaxation, 2) profound (99.5%) and selective inhibition of crural diaphragmatic activity, and 3) a previously unrecognized dorsal movement of the gastroesophageal junction (mean 1.3 cm) demonstrated by implanted radiological markers. The patterns associated with spontaneous acid and gas reflux were indistinguishable from those induced by gastric distension. Costolumbar diaphragmatic activity was stable up until the instant of sphincter opening, when there was a single costolumbar contraction of short duration and high amplitude. Esophageal shortening did not occur before reflux. Reflux that occurred after atropine-induced inhibition of lower esophageal sphincter tone to < 2 mmHg was intermittent and coincided with selective crural inhibition. These studies demonstrated that selective crural inhibition is a prerequisite for gastroesophageal reflux and suggest that the crural diaphragm is an important factor for the maintenance of gastroesophageal competence.

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